Advanced Glycation End Products Inhibit the Expression of Collagens Type I and III by Human Gingival Fibroblasts

Ren, Luping; Fu, Yao‐Shi; Deng, Yuquan; Qi, Liu-ying; Li, Jin

doi:10.1902/jop.2009.080669

Cited by 37 publications

(27 citation statements)

References 42 publications

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“…This effect is likely due to the ability of AGEs to inhibit cell proliferation, downregulate collagen expression, induce collagen cross-linking and inflammatory responses that, in turn, impair wound healing. 57–59 Thus, in Akita −/− mice, hyperglycemia likely leads to accumulation of AGEs in pulp and periodontal structures and compounds the detrimental effects of hyperglycemia on dental tissues.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Yeh

Harris

Mohan

et al. 2012

Laboratory Investigation

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Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Yeh

Harris

Mohan

et al. 2012

Laboratory Investigation

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“…An example of this product is the above reported HbAlc. Subsequently, a complex series of molecular reactions resulting in the formation of molecules called "Advanced Glycosylation End products" (AGEs) take place [98,99]. The AGEs are irreversible and belong to a heterogeneous group including carboxymethyllysine (a modified amino acid that accumulates with age in human lens proteins and collagen), the more predominant AGE in diabetic patients and related with tissue aging [100].…”

Section: Diabetes and Periodontitismentioning

confidence: 99%

“…Summarizing, hyperglycemia determines AGE deposition in the collagenous matrix of the periodontal ligament and the alveolar bone matrix, and in BM of gingival capillary walls [99] associated to increased oxidation, altered PMN functions and atheroma formation, interferes with normal periodontal wound healing, perpetuating periodontal disease in the diabetics [84,92].…”

Section: Diabetes and Periodontitismentioning

confidence: 99%

Does It Make Sense that Diabetes is Reciprocally Associated with Periodontal Disease?

Santacroce¹,

Carlaio²,

Bottalico³

2010

EMIDDT

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Epidemiological studies indicated that more than 15% of the population in western countries suffer because of severe forms of periodontitis, In this respect, the recognition of the relationship between oral and systemic health is growing, thus receiving remarkable interest in scientific literature. In fact, periodontitis may increase the risk for a group of life-threatening conditions such as atherosclerosis, stroke or low birth weight. The American Diabetes Association has reported that individuals with uncontrolled diabetes (defined as 200mg/dL of glucose on three consecutive readings) undergo an increased risk of infections, abnormal wound healing and consequent increased recovery time. Moreover, diabetics may be more likely to develop periodontal and cardiovascular disease than non diabetics, if note. History of poorly controlled chronic periodontal disease can alter diabetic/glycemic control. This may originate from a likely continuous passege of bacterial toxins and/or bacteria into the bloodstream, and/or from an exaggerated release of inflammatory mediators. This review is aimed at elucidating the connections between the status of oral health and glycemic control in diabetes.

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“…Increased AGEs are correlated to inhibited expression of collagen type I and type III in human gingival fibroblasts [21]. Several studies have shown that patients with incisional hernia have a decreased collagen type I/III ratio in the scar of the abdominal wall, the skin and in the uninjured fascia laterally to the scar postoperatively [8, 22–24].…”

Section: Discussionmentioning

confidence: 99%

Advanced glycation end products as a biomarker for incisional hernia

Harlaar

Eker

Vakalopoulos

et al. 2017

Hernia

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BackgroundIncisional hernia is one of the most frequent complications after abdominal surgery, with incidences up to 30%. A reliable biomarker for the prediction of this complication is lacking. Advanced glycosylation end products (AGEs), also known as non-enzymatic collagen crosslinks, are correlated with aging, smoking, hyperglycemia, hyperlipidemia and oxidative stress. In this study the accumulation of AGEs and the relation between AGEs and incisional hernia were investigated.Materials and methodsIn an exploratory case–control study, 23 patients with incisional hernia after midline incision were compared with 17 patients without clinical or radiological signs of incisional hernia after midline incision, AGEs were measured using a Skin Auto Fluorescence (SAF)-reader.ResultsTwenty-three patients with a clinically significant incisional hernia and 17 control patients were included. The study groups had significant differences in mean BMI. There was a significant difference between mean AGEs in patients with and without incisional hernia after midline incision (3.00 ± 0.15 vs. 2.56 ± 0.11, T test p = 0.03).ConclusionAGE accumulation measured in the skin indirectly with autofluorescence might be associated with incisional hernia. Prospective larger trials should confirm this finding.

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Advanced Glycation End Products Inhibit the Expression of Collagens Type I and III by Human Gingival Fibroblasts

Cited by 37 publications

References 42 publications

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice

Does It Make Sense that Diabetes is Reciprocally Associated with Periodontal Disease?

Advanced glycation end products as a biomarker for incisional hernia

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